Q10 and selenium protect the heart

April 23, 2023

Supplementation of Q10 and Selenium over a 4-year period
could halve cardiovascular mortality.

A  short  time ago a very important scientific article was published.

The article was an offshoot of the sensational article by researcher Dr. Urban Alehagen and colleagues from 2015, who showed massive cardiovascular protection with supplementation of Q10 in combination with selenium.
Alehagen and colleagues then carried out a follow-up of this study, but not only that. They have also sought to dig into the actual cause of this positive effect, which was a halving of cardiovascular mortality after 4 years of supplementation.

The logic is straight to the point. The vast majority of cardiovascular diseases are caused by atherosclerosis, and this is caused by a combination of inflammation, i.e. a local response to tissue damage and oxidation (here rancidity). Without these two factors, atherosclerosis does not occur.

Briefly, the mechanism is that oxidation turns LDL3 cholesterol rancid, which is thereby “eaten” by a type of white blood cells called monocytes via a structure on the cell surface called a “scavenger receptor”. This means that LDL cholesterol is directed around the usual LDL receptor, which could otherwise easily block intake. But the scavenger receptor cannot stop its intake of LDL cholesterol if it is oxidized, because LDL in this form acts as a free radical. And that is exactly what the scavenger receptor is designed to let into the monocyte. However, since the intake cannot stop, even though the monocyte is probably so crowded, it swells up and is seen under the microscope as a large white blob. And when there are many of these monocytes together, it looks like foam. Therefore, these “overfed” monocytes are called “foam cells”.
Oxidation is thus required for a monocyte to become a foam cell.
When the monocyte circulates in the bloodstream, it will react if it finds an area, e.g. the blood vessel wall, where there is inflammation, e.g. due to high blood pressure. The monocyte will search for the inflamed area, penetrate the vessel wall (into the subendothelial layer), where it will perish and leave behind a fatty layer of oxidized LDL3 cholesterol. This will increase inflammation and attract even more foam cells, which in turn perish, leaving behind more of the rancid fat, which is gradually consolidated by fibrin and finally stabilized by calcium, which is the last step in atherosclerosis.

The entire above process will not take place unless there is both increased inflammation and oxidation.
And precisely selenium and Q10 inhibit both inflammation and oxidation. Therefore, it is perhaps not so strange that they prevent cardiovascular disease and reduce the risk of dying from it.

The body’s cells produce energy in order to function, and this energy requires Q10 in the cells’ internal power plant, the mitochondria.
Unfortunately, there is a natural decline in the body’s production of Q10 as we age, and it is therefore natural to supplement this.
Q10 is a substance that the body produces in almost the same way as it produces cholesterol. Q10 and cholesterol are actually sister molecules that look very similar. So when you take a cholesterol-lowering medication, you also lower the production of Q10. You should therefore be aware that you often lack Q10 if you take cholesterol-lowering medication.

Selenium is a substance that we absolutely must not lack, and numerous studies have confirmed over the years that selenium deficiency can lead to, among other things, heart failure, cancer, metabolic disorders, arthritis, childlessness, atherosclerosis, increased inflammation and a number of immunological failures, which were particularly relevant in the corona era.
There are thousands of articles that cement heavy research into selenium, such as a study of selenium deficiency related to cardiovascular disorders and inflammatory conditions. Since cardiovascular disorders are also initiated by inflammation, it is natural to investigate this together.
Previous studies have also shown that low selenium in the blood was the cause of increased inflammation, increased risk of cardiovascular disease and early death.

The current study mentioned above is also primarily aimed at finding the biochemical mechanism behind this effect.

As mentioned above, it is based on Alehagen and colleagues’ article from 2015, and it is evidence with a very high degree of reliability, as it was a double-blind, randomized, prospective study. The participants were healthy elderly with an average age of 76 years. 165 received 200µg Selenium + 200mg Q10 daily, and 161 received placebo. The treatment lasted 4 years, after which various parameters were measured.
They were particularly interested in measuring the change in Sirtuin1, an enzymatic protein (deacetylase), which is important for the survival of cells when they are exposed to oxidative stress, because Sirtuin1 increases the effect of certain antioxidants.
But not only that. Sirtuin1 also inhibits the so-called NFκB signal, which is a substance that otherwise produces a strong inflammatory response.
So if you can increase Sirtuin1, you will thereby be able to inhibit inflammation and oxidation, – in other words, the two factors, which are mainly responsible for, among other things, cardiovascular diseases.
After a 4-year intervention period, the SIRT1 concentration was found to be significantly increased (from 252 to 469 ng/ml) in the active group and decreased (from 269 to 190 ng/ml) in the placebo group.
In a 10-year follow-up period, 25 in the active group and 52 in the placebo group died of cardiovascular disease, and the 77 who died had significantly lower SIRT1 concentration than the rest.
A small wrinkle in the study is that the so-called microRNA is also affected in a direction that inhibits the aging of the cardiovascular system. Micro-RNA contributes to the regulation of the gene activity. This has very far-reaching consequences for epigenetics, that is different modifications of DNA, which can turn genes on or off, and will of course be explored intensively in the future.

In this scientific trial, Alehagen and colleagues have shown that just 4 years of Selenium and Q10 supplementation inhibits oxidation and inflammation, and halves cardiovascular mortality over a 10-year period.

Now that selenium and Q10 are effective in inhibiting oxidation and inflammation, it is not surprising that they can halve the risk of dying from cardiovascular disease.
It is more strange that this is not standard advice from the medical profession when the evidence is so solid.

Take care of yourself and others.

Claus Hancke MD
Specialist in general medicine

Vitamin D Can Be Used As Heart Medicine

May 23, 2006

The warnings against direct sunlight in the summer should be taken with a grain of salt. The vitamin D synthesized in the skin in the wonderful sunshine, prevents, amongst other things, weakening of the heart, if we look at the latest research.

Sooner or later in the course of the summer a dermatologist will appear on television to warn against direct exposure to the sun. It may lead to skin cancer and also threatening is the feared, deadly birthmark cancer, the incidence of which has risen dramatically in step with more and more people desiring a tan. This is partly true.

On the other hand it is prudent to be skeptical when someone advices us to act against what is natural. Can it really be true that the sun is so dangerous when people in our part of the world have been far more exposed to the sun through thousands of years?

Vitamin D is made in the skin when it is in the sunlight, but not from September till May, when the sun is too low on the horizon to be used for this in our part of the world. Since our diet only contains minimal amounts of this vitamin, in the wintertime we use the vitamin which has been built up in the skin in the course of the summer. During the winter approximately 85 % of the daily D-vitamin usage is taken from reserves, even in cases where the diet is rich in D-vitamin. All in all, approximately 100 mcg. is used in a day.

But what happens if the reserves are too small?

In the past half-year a number of studies have shed light over the mysteries of vitamin D. According to one study, the vitamin can help against tuberculosis, which we know was a widespread disease in the 19th and beginning of the 20th century, when many people lived under dire conditions in the cities.

Another study of over 14,000 Americans showed that the people with the largest D-vitamin reserves generally had far better lung function than those with the smallest stores. The difference is as big as the difference between ex-smokers and people who have never smoked before. A possible explanation is that the D-vitamin secures the necessary repairs of worn-out cells.

At about the same time, one of the veterans of vitamin-D research, the American Cedric Garland, concluded that now the proof that vitamin D protects against cancer (especially breast cancer, cancer of the colon and prostate cancer) was very strong. Strong enough to make him regard the connection as definite. He has reviewed all relevant research done since 1966.

Weak Heart and Arthritis
His claims can be compared to the fact that David Feldman of Stanford University now wants to conduct an experiment with calcitriol (the active form of vitamin D, which is made in body from vitamin D in the skin or the food) and ordinary arthritis medication against prostate cancer. In laboratory studies he has found that calcitriol slows the growth of prostate cancer by 25 %, while the combination with arthritis medication slows it by 70 %. A true break-through if it is true.

Everyone knows that vitamin D is necessary for the bones, but it is also necessary for the muscles. A deficiency leads to both muscle pain, weak muscles and for example, a tendency to fall in the elderly. But what about the heart? The heart is also a muscle, and weakening of the heart (cardiac insufficiency) because of atherosclerosis or increased blood pressure occurs in as many as 50,000 Danes. It is a dangerous condition with a high mortality rate.

A German study of 123 patients with a weak heart showed that on average they had quite small amounts of vitamin D in their blood stream, close to a deficiency in the traditional sense. Half of them were given supplements of 50 mcg. D3-vitamin each day for nine months. This is five times as much as the elderly are traditionally recommended given, and is also the upper limit, of what is not dangerous to ingest.
The study was too small to show a difference in mortality, but it did show something interesting. It concerns the protein TNF-alpha, which is produced by the white blood cells in connection with inflammation. TNF-alpha is meant to be a major cause of weakening of the heart. In the patients left untreated, the blood’s content of this protein increased by 5 %. In those treated, there was no worsening. This indicates a stabilizing effect on the inflammation.

This is especially interesting for another reason. TNF-alpha is an important cause of pain and swelling in arthritis. So important that new types of arthritis medication, which blocks TNF-alpha, fittingly, are considered wonder-drugs. If vitamin D decreases the effect of TNF-alpha on the weakened heart, maybe the same happens in arthritic joints. This would also confirm the old assumption that vitamin D protects against arthritis.

When in the sun, one should be sensible and avoid sunburns. Stay in the shadow if the sun is very strong and do not lie about for hours in the sun all covered up in greasy sun lotion.

Also important to know is that it is a risk rather than a virtue to stay out of the sun in the summer.

By: Vitality Council

1. Schleithof S S et al. Vitamin D supplementation improves cytokine profiles in patients with congestive heart failure: A double blind randomized placebo-controlled trial. Am J Clin Nutr 2006;83:754-9
2. Heaney R et al. Human serum 25-hydroxycholecalciferol response to extended oral dosing with cholecalciferol. Am J Clin Nutr 2003;77:304-10.
3. Moreno J, Krishnan AV, Feldman D. Molecular mechanisms mediating the anti-proliferative effects of Vitamin D in prostate cancer. J Steroid Biochem Mol Biol. 2004 Nov;92(4):317-25